The present invention deals with treatment of heart disease. More particularly, the present invention deals with a system and method for treating heart disease by regulating blood flow in the vasculature.
Congestive heart failure is a common heart disease. The prevalence of incidents of congestive heart failure has recently increased, and there is considerable morbidity and mortality associated with its diagnosis. In fact, congestive heart failure is an extremely lethal disease with an estimated five year mortality for a vast majority of both men and women who encounter the disease.
Congestive heart failure results from loss of, or impairment of, normal heart function. This loss or impairment reduces cardiac output. This, in turn, results in a reduction in both blood flow and blood pressure in the kidneys. This reduction in flow and pressure causes a renin-angiotensin response that exacerbates congestive heart failure.
Briefly, as blood flow and pressure is reduced in the kidneys, cells in the kidneys referred to as juxtaglomerular apparatus secret an enzyme referred to as renin into the blood. The enzyme renin cleaves a ten-amino acid polypeptide called angiotensin I from a plasma protein in the blood called angiotensinogen. A converting enzyme in the blood removes two amino acids from the angiotensin I polypeptide leaving an eight amino acid polypeptide called angiotensin II. Angiotensin II has numerous effects on the smooth muscle layers of arterioles, including causing vasoconstriction. Further, an indirect effect of an increase in angiotensin II increases blood volume. Blood volume is increased because angiotensin II stimulates secretion of aldosterone from the adrenal cortex which, in turn, causes an increase in salt and water retention in the kidneys. Angiotensin II also stimulates thirst centers in the hypothalamus causing more water to be ingested. The increase in blood volume and the corresponding vasoconstriction cause an increase in blood pressure and hence a volume overload on the heart which causes further deterioration of the heart condition.
Another response is also related to congestive heart failure. Baroreceptors, referred to as stretch receptors, reside in the aortic arch and carotid sinuses. The baroreceptors are essentially pressure sensors sensing blood pressure in that area. The baroreceptors provide physiological feedback in two ways. First, in response to a reduction in blood pressure, the baroreceptors provide a neurohormonal feedback response which acts to increase the heart rate in an attempt to increase cardiac output. The increased heart rate causes the heart to work harder which, in turn, causes the heart muscle to stretch further. Also, a reduction in pressure caused by a reduction in cardiac output causes the baroreceptors to provide a feedback response which acts to constrict the distal vasculature thus increasing pressure in that area.
It can thus be seen that impairment of heart function can lead to a cyclical feedback response which increases, rather than reduces, the impairment. Such a cyclical feedback response is sometimes referred to as a cascade.
For instance, if the heart muscle is stressed, the heart works harder and begins to stretch. This reduces the efficiency of the heart in the following way. Muscles are thought of as being composed of many fibers which contract and lengthen to accomplish muscular action. Each fiber includes many densely packed subunits referred to as myofibrils which are on the order of 1 xcexcm in diameter and extend in parallel from one end of the muscle fiber to the other. Each myofibril has spaced regions of thick filaments (about 110 xc3x85 thick) and thin filaments (about 50-60 xc3x85 thick) The thick filaments are formed of a protein, myosin, and the thin filaments are formed of a protein, actin. The actin and myosin filaments overlap in regions periodically spaced along the myofibrils. The units in the repeated overlapping pattern are referred to as sarcomeres.
Contraction of a muscle fiber results from shortening of the myofibrils which form the muscle fiber. The myofibrils are shortened, but the individual filaments in the myofibrils do not decrease in length. Instead, the actin and myosin filaments slide longitudinally relative to one another to shorten the overall length of the myofibrils. Sliding occurs as a result of cross-bridges extending from the myosin toward the actin attaching to the actin at bonding sites. The cross bridges are oriented to draw overlapping actin filaments on either longitudinal side of the myosin filament toward the longitudinal center of the myosin filament. When the muscle fiber is stretched such that the actin and myosin only overlap a short distance, only a small number of cross-bridges are available for bonding to the adjacent actin, and contraction is highly inefficient. When the muscle is stretched to a point where the actin and myosin filaments no longer overlap, contraction is rendered impossible.
This inefficient or impaired heart function causes blood pressure in the areas of both the kidneys and the baroreceptors to decrease. The feedback response generated by the kidneys causes further overload and stress on the heart. The feedback response generated by the baroreceptors causes increased heart rate. Both of these feedback responses cause the heart to work harder, causing further stretching of the heart muscle and thus leading to greater inefficiencies. In response, the feedback responses become even more acutexe2x80x94and the cascade continues.
This cascade effect, which is a natural progression of congestive heart failure, leads to increased muscle mass and stretching of the heart muscle fibers which, in turn, leads to muscular hypertrophy,of the left ventricle. The hypertrophy is a compensatory mechanism which, if maintained at a given level such that muscle fibers maintain inherent contractile properties (i.e., actin-myosin overlap), can be beneficial for maintaining proper heart function. However, prolonged and continuous stretching causes muscular fatigue and reduced muscle performance as explained by the known Frank-Starling mechanism.
An apparatus and method restrict elongation of heart muscle tissue in a wall of a heart having a chamber. A plurality of biocompatible and implantable elongate strips are configured to be connected to the heart wall and disposed about the chamber such that the elongate strips are arranged in spaced relation to one another. The elongate strips are bendable and are sufficiently resistant to elongation such that natural stretching of the heart wall does not cause elongation of the plurality of strips.